NAAA-regulated lipid signaling governs the transition from acute to chronic pain

Yannick Fotio, Kwang-Mook Jung, Francesca Palese, Andre Obenaus, Alex Mabou Tagne, Lin Lin, Tarif Ibne Rashid, Romario Pacheco, Amandine Jullienne, Jade Ramirez, Marco Mor, Gilberto Spadoni, Cholsoon Jang, Andrea G Hohmann, Daniele Piomelli. Sci Adv. 2021 Oct 22;7(43):eabi8834.

Laboratory studyOther animalsWith Small-molecule NAAA inhibitors, which raise the body's own palmitoylethanolamide; PEA itself was not given

This study tested palmitoylethanolamide together with Small-molecule NAAA inhibitors, which raise the body's own palmitoylethanolamide; PEA itself was not given. Its results cannot be assigned to palmitoylethanolamide alone. More combination studies.

Design

Laboratory study

Subjects

Male and female mice with peripheral tissue injury; numbers not stated in the abstract

Dose used in the study

Not stated in the abstract

Duration

NAAA disabled during a 72-hour window after injury

What was measured

Development of chronic pain after tissue injury; spinal cord metabolism (aerobic glycolysis versus mitochondrial respiration); PPAR-alpha dependence.

What the authors reported

Disabling NAAA in the spinal cord within 72 hours of injury halted the development of chronic pain in male and female mice. The effect depended on PPAR-alpha and involved a shift in local metabolism from aerobic glycolysis back to mitochondrial respiration.

Limits of this study

A mouse study; it cannot show effect in people. No palmitoylethanolamide was given; NAAA inhibition raised the body's own PEA. Conflicts not stated in the abstract; the senior author holds patents on NAAA inhibitors in related papers.

Source

PubMed 34678057 · doi:10.1126/sciadv.abi8834

Entry checked against the abstract on PubMed on 2026-09-22. The dose shown is the dose the researchers used. It is not a recommendation. How to read this page.